Melatonin and Associated Signaling Pathways that Control Normal Breast Epithelium and Breast Cancer

2011 ◽  
Vol 16 (3) ◽  
pp. 235-245 ◽  
Author(s):  
Steven M. Hill ◽  
David E. Blask ◽  
Shulin Xiang ◽  
Lin Yuan ◽  
Lulu Mao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Signaling Pathways ◽  
Normal Breast ◽  
Breast Epithelium ◽  
Normal Breast Epithelium

scholarly journals DNA Methylation and Breast Cancer Risk: An Epigenome-Wide Study of Normal Breast Tissue and Blood

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3088 ◽  
Author(s):  
Kaoutar Ennour-Idrissi ◽  
Dzevka Dragic ◽  
Elissar Issa ◽  
Annick Michaud ◽  
Sue-Ling Chang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Breast Tissue ◽  
Normal Breast Tissue ◽  
Normal Breast ◽  
Breast Epithelium ◽  
Normal Breast Epithelium ◽  
Differentially Methylated Genes

Differential DNA methylation is a potential marker of breast cancer risk. Few studies have investigated DNA methylation changes in normal breast tissue and were largely confounded by cancer field effects. To detect methylation changes in normal breast epithelium that are causally associated with breast cancer occurrence, we used a nested case–control study design based on a prospective cohort of patients diagnosed with a primary invasive hormone receptor-positive breast cancer. Twenty patients diagnosed with a contralateral breast cancer (CBC) were matched (1:1) with 20 patients who did not develop a CBC on relevant risk factors. Differentially methylated Cytosine-phosphate-Guanines (CpGs) and regions in normal breast epithelium were identified using an epigenome-wide DNA methylation assay and robust linear regressions. Analyses were replicated in two independent sets of normal breast tissue and blood. We identified 7315 CpGs (FDR < 0.05), 52 passing strict Bonferroni correction (p < 1.22 × 10−7) and 43 mapping to known genes involved in metabolic diseases with significant enrichment (p < 0.01) of pathways involving fatty acids metabolic processes. Four differentially methylated genes were detected in both site-specific and regions analyses (LHX2, TFAP2B, JAKMIP1, SEPT9), and three genes overlapped all three datasets (POM121L2, KCNQ1, CLEC4C). Once validated, the seven differentially methylated genes distinguishing women who developed and who did not develop a sporadic breast cancer could be used to enhance breast cancer risk-stratification, and allow implementation of targeted screening and preventive strategies that would ultimately improve breast cancer prognosis.

scholarly journals Gene expression abnormalities in histologically normal breast epithelium of breast cancer patients

2007 ◽  
Vol 122 (7) ◽  
pp. 1557-1566 ◽  
Author(s):  
Anusri Tripathi ◽  
Chialin King ◽  
Antonio de la Morenas ◽  
Victoria Kristina Perry ◽  
Bohdana Burke ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Patients ◽  
Normal Breast ◽  
Breast Cancer Patients ◽  
Breast Epithelium ◽  
Normal Breast Epithelium

Gene expression abnormalities in histologically normal breast epithelium from patients with luminal type of breast cancer

2014 ◽  
Vol 42 (5) ◽  
pp. 977-988 ◽  
Author(s):  
Pavol Zubor ◽  
Jozef Hatok ◽  
Petra Moricova ◽  
Karol Kajo ◽  
Ivana Kapustova ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Normal Breast ◽  
Breast Epithelium ◽  
Normal Breast Epithelium ◽  
Luminal Type

scholarly journals EZH2 protein expression in normal breast epithelium and risk of breast cancer: results from the Nurses’ Health Studies

2017 ◽  
Vol 19 (1) ◽  
Author(s):  
Francisco Beca ◽  
Kevin Kensler ◽  
Benjamin Glass ◽  
Stuart J. Schnitt ◽  
Rulla M. Tamimi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Protein Expression ◽  
Normal Breast ◽  
Breast Epithelium ◽  
Normal Breast Epithelium ◽  
Health Studies

Scotin expression and survival in breast cancer

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e22006-e22006
Author(s):  
J. Bourdon ◽  
A. Diot ◽  
B. Vojtesek ◽  
S. Bray ◽  
L. Jordan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mrna Expression ◽  
Significant Proportion ◽  
Normal Breast ◽  
Breast Cancers ◽  
Wild Type ◽  
Poor Survival ◽  
Breast Epithelium ◽  
Normal Breast Epithelium ◽  
Cytoplasmic Staining

e22006 Background: The Scotin gene (3p21.3) is directly trans-activated by p53 in response to ionising radiation and produces a 25kD trans-membrane protein located in the endoplasmic reticulum and nuclear membrane which induces a caspase- dependent apoptosis. This study examines the expression of scotin and scotin isoforms in breast cancer in relation to clinical and pathological parameters. Methods: Scotin was examined in 145 breast cancers by DNA sequencing, nested PCR for mRNA expression and using novel antibodies to scotin (pantropic), the C-terminal or N-terminal domain, and the scotin-5 isoform with western blotting and immunohistochemistry on a tissue microarray of breast cancers. Results: Scotin was mutated in 10% of cancers and mRNA expression lost in a further 10%. Moreover, Scotin-5 was expressed in 40% of cancers, while it was not detectable in normal breast epithelium. We established that Scotin-5 is anti-apoptotic and inhibits scotin-mediated apoptosis. Cytoplasmic staining of scotin on TMAs demonstrated that loss of scotin expression was associated with earlier relapse (Mantel-Cox log rank p<0.01) and poor survival (Mantel-Cox log rank p<0.002). Furthermore, loss of Scotin expression identified 50% of the WTp53 patients or 50% of the ER+ patients who also had a poor survival. Conclusions: Scotin may be used as an independent biomarker in breast cancer. Loss of Scotin function may account for a significant proportion of p53 malfunction even in the presence of wild type p53 in breast cancer and adds a further level of complexity to p53 directed therapy in breast cancer. No significant financial relationships to disclose.

Abstract 1071: Age-dependent DNA methylation in normal breast epithelium and breast cancer

2015 ◽  
Author(s):  
Shoghag B. Panjarian ◽  
Carolyn Slater ◽  
Jozef Madzo ◽  
Jaroslav Jelinek ◽  
Xiaowei Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Normal Breast ◽  
Breast Epithelium ◽  
Normal Breast Epithelium ◽  
Age Dependent

scholarly journals Cellular calcium dynamics in lactation and breast cancer: from physiology to pathology

2014 ◽  
Vol 306 (6) ◽  
pp. C515-C526 ◽  
Author(s):  
Brandie M. Cross ◽  
Gerda E. Breitwieser ◽  
Timothy A. Reinhardt ◽  
Rajini Rao
Keyword(s):  
Breast Cancer ◽  
Functional Module ◽  
Normal Breast ◽  
Calcium Dynamics ◽  
Breast Epithelium ◽  
Normal Breast Epithelium ◽  
Pathological Characteristics ◽  
Intracellular Ca ◽  
Tumor Growth And Metastasis ◽  
Therapeutic Possibilities

Breast cancer is the second leading cause of cancer mortality in women, estimated at nearly 40,000 deaths and more than 230,000 new cases diagnosed in the U.S. this year alone. One of the defining characteristics of breast cancer is the radiographic presence of microcalcifications. These palpable mineral precipitates are commonly found in the breast after formation of a tumor. Since free Ca2+ plays a crucial role as a second messenger inside cells, we hypothesize that these chelated precipitates may be a result of dysregulated Ca2+ secretion associated with tumorigenesis. Transient and sustained elevations of intracellular Ca2+ regulate cell proliferation, apoptosis and cell migration, and offer numerous therapeutic possibilities in controlling tumor growth and metastasis. During lactation, a developmentally determined program of gene expression controls the massive transcellular mobilization of Ca2+ from the blood into milk by the coordinated action of calcium transporters, including pumps, channels, sensors and buffers, in a functional module that we term CALTRANS. Here we assess the evidence implicating genes that regulate free and buffered Ca2+ in normal breast epithelium and cancer cells and discuss mechanisms that are likely to contribute to the pathological characteristics of breast cancer.

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